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PubMed1997

Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model.

Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-alpha). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1-2) and chronic phases (week 3-4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.

Acute Disease↗
PubMed1983

Foetal and maternal magnesium metabolism: effect of magnesium deficiency and isoproterenol.

Pregnant rats were fed diets with an Mg2+ content of 40, 12, 6 and 3 mmol/kg from day 10-19 of pregnancy. There was a linear correlation of non-protein bound Mg2+ between foetal and maternal serum, between amniotic fluid and maternal serum, and between foetal serum and amniotic fluid, the ratios being 2.7, 2.0 and 1.3 respectively, indicating active transport of Mg2+ up to a constant concentration gradient by the placenta. In hearts, increases of Na+ and Ca2+, and decreases of Mg2+ and K+ were observed only in the group receiving the lowest Mg2+ supply. After i.v. injection of MgCl2 to pregnant rats, Mg2+ was slowly transported from maternal to foetal serum and more slowly into the amniotic fluid. The effect of isoproterenol on cardiac electrolyte content in pregnant rats was less than in non-pregnant rats, and the effect of isoproterenol in foetal rats was smaller than in maternal rats. These results are explained by inactivation of isoproterenol in the placenta, by the small diaplacental transport of isoproterenol and by a smaller isoproterenol-stimulation of foetal cardiac adenylate cyclase.

Amniotic Fluid↗
PubMed1977

Plasma parathyroid hormone and calcitonin levels in hypocalcaemic magnesium-deficient calves.

Mg deficiency was experimentally induced in 3 calves given Mg-deficient semi-synthetic milk (10 mg of Mg/l of milk). Three control calves received the same milk supplemented with Mg (190 mg of Mg/l of milk). Calcium and vitamin D contents of this milk were similar to that of natural milk. Daily weight gain in control calves was similar to that observed in calves given natural milk. The daily weight gain of Mg-deficient calves was not statistically different from that of control calves during the first 6 weeks of Mg-deficiency. Then clinical symptoms of Mg-deficiency appeared (loss of appetite, nervousness, tetany crises). In these Mg-deficienct animals a fall in plasma magnesium level, followed by hypophosphataemia and then by hypocalcaemia was observed. During the whole experimental period plasma CT and plasma PTH levels were not statistically different in Mg-deficient and in control calves. These results show that the hypocalcaemia observed in Mg-deficient calves was due neither to an increase in CT secretion nor to a decrease in PTH secretion. Nevertheless, the parathyroid glands from these animals seem unable to react satisfactorily to the hypocalcaemia induced by Mg-deficiency.

Animals↗
PubMed1989

Induction of a rat T cell lymphoma-leukemia by magnesium deficiency--a study of fetal defense against maternal neoplasia.

If Sprague-Dawley rats, 25-30 days old, are fed a diet containing 4-5 mg% of Mg, about 25% of survivors develop a large tumor of the thymus within 6-12 weeks. The tumor is composed of lymphoblasts, which seem to arise from the thymic reticuloendothelial system and, at times, disseminate as an acute T cell lymphoma-leukemia of unknown etiology. If the tumor cells are transmitted intraperitoneally to rats, 14-16 days pregnant, a local invasive and generalized disease is established in the mother but not in the fetuses or their domain. However, if the neoplastic cells are injected into the fetal domain, they colonize the fetal tissues. The colonization by tumor cells is most impressive in the extravascular structure of the placental labyrinth but not in the placental syncytiotrophoblastic zone at the maternal-placental junction. This raises the question as to whether this zone may functionally mediate not only the well-known absolute intrauterine fetal defense against maternal metastatic neoplasia, but also the defense of the fetus against maternal immunologic rejection.

Aging↗
PubMed2000

Magnesium deficiency modulates the insulin signaling pathway in liver but not muscle of rats.

Altered insulin secretion and sensitivity have been observed in Mg-deficient animals. However, the effects of Mg deficiency and supplementation on intracellular signaling events triggered by insulin are unknown. Therefore, we studied the early steps of insulin action in muscle and liver of rats fed Mg-deficient (DF-6, DF-11) or control (CO-6, CO-11) diets for 6 or 11 wk, respectively, and Mg-deficient or control diets for 6 wk, followed by Mg supplementation for 5 wk (SDF and SCO groups, respectively). There were no differences in the glucose disappearance rate (K(itt)) or insulin signaling between CO-6 and DF-6 rats. Between the two groups of rats fed for 11 wk, the DF-11 group had a significantly greater K(itt). SDF and SCO rats had K(itt) that did not differ from CO-11 rats, but that were significantly lower than in DF-11 rats. In the latter rats, insulin receptor and insulin receptor substrate-1 protein and phosphorylation levels were elevated in liver and there was a greater association between the insulin receptor substrate-1 and p85 subunit of phosphatidyl-inositol 3-kinase compared with CO-11 rats. There were no differences in the early steps of insulin action in SDF and control rats. These results suggest that the normal insulin sensitivity maintained by Mg supplementation and the increased insulin sensitivity produced by a long period of Mg deprivation may result, at least in part, from alterations in or maintenance of the early molecular steps of insulin action in hepatic tissue.

Analysis of Variance↗
PubMed1988

Structural changes in lungs of magnesium-deficient weanling rats dying spontaneously or after spontaneous recovery from the seizure-shock episode. Possible methods for sudden infant death syndromes.

A light and electron microscopic study of Mg-deficient weanling rats showed structural changes of the lungs associated with the audiogenic seizure-shock episode, and with sudden, spontaneous death or spontaneous recovery after the shock episode. Pathogen-free weanling males were fed a Mg-deficient (Mg-0) or Mg-sufficient (Mg-100) diet and were raised in a gnotobiotic environment. Mg-100 rats (n = 16), unstressed or stressed with noise or strychnine, showed normal lungs. Mg-0 rats (n = 20) experienced audiogenic seizure-shock, followed by hyperventilation with tonic-clonic hyperextension of the back and extremities. The lungs of Mg-0 rats sacrificed during shock showed marked hemorrhage, including petechiae; edema; and atelectasis. Eight that died after a post-shock period of hyperventilation and hyperextension of the spine showed partial recovery of the pulmonary lesion; they showed well-expanded lungs, pleural petechiae, persistent congestion, with mild to moderate pathology. Mg-0 rats killed for study 2 days after the seizure-shock episode showed few small areas of residual lung pathology. Ultrastructural changes after Mg-O shock included aggregated platelets, leukocytes, and occasional reticulocytes in congested capillaries. Surfactant was disrupted during Mg-0 seizure-shock, but a layer closely applied to the surface of the epithelium was evident 2 days after shock. Mg-0 rats dying spontaneously showed nonspecific structural changes of the lung similar to changes reported in the sudden infant death syndrome (SIDS).

Acoustic Stimulation↗
PubMedDate not supplied

Sinoatrial automaticity and transmembrane potentials in hamsters on a magnesium-deficient diet.

We studied the effects of moderate Mg deficiency on sinus node automaticity and atrial muscle transmembrane potential in hamsters. The Mg-deficient hamsters (Mg-D) were fed a diet containing less than 2.0 mmol/kg Mg (0Mg) for 7 days. They were then fed 0Mg enriched with 10 mmol/kg Mg acetate for 12 days. Control animals (Mg-N) were fed a Mg-sufficient diet consisting of 0Mg supplemented with 100 mmol/kg Mg acetate. Sinoatrial preparations from Mg-N and Mg-D animals were superfused in vitro with Tyrode solution at 36 degrees C. Transmembrane potentials were recorded using intracellular microelectrodes. Preparations from Mg-D hamsters beat at a more rapid spontaneous rate than did those from Mg-N animals. A decrease in [Mg]0 enhanced the automaticity of Mg-N preparations, but not of Mg-D preparations. The negative chronotropic action of carbamycholine (CBL) was greater in the Mg-D than in the Mg-N preparations. When driven at a constant rate, the atrial muscle fibers of Mg-D hamsters repolarized more rapidly than did those of the Mg-N group. The resulting difference in the action potential duration (APD) was independent of membrane resting potential (MRP), amplitude of the action potential (AAP), and velocity of depolarization during phase 0 (Vmax), which were the same in both groups of preparations. The APD was shortened to a similar extent, proportionally, by 100 nM CBL in both preparations, while MRP, AAP, and Vmax remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1998

Daily magnesium supplementation effect on magnesium deficiency in rats during prolonged restriction of motor activity.

The objective of this investigation was to evaluate the effect of magnesium (Mg) supplements in rats during prolonged restriction of motor activity (hypokinesia [HK]) and in the presence of Mg deficiency, which is characterized by increased rather than decreased plasma Mg concentration, as occurs in ambulatory conditions. The studies were performed during 98 days of HK on 100 13-week-old Sprague-Dawlay male rats weighing 360 to 390 g. They were equally divided into four groups: (1) unsupplemented control animals (UCA), (2) unsupplemented hypokinetic animals (UHA), (3) supplemented control animals (SCA), and (4) supplemented hypokinetic animals (SHA). For the simulation of the hypokinetic effect, SHA and UHA were kept for 98 days in small individual wood cages that restricted their movements in all directions without hindering food and water intake. The SCA and SHA took daily with their food an additional 0.35 mg of Mg. Before and during the hypokinetic period of 98 days, Mg in plasma, urine, and feces, balance of Mg, food intake of Mg, and body weight were determined at different intervals. In SHA and UHA, plasma Mg concentration and excretion of Mg in urine and feces increased significantly compared with SCA and UCA. Magnesium balance was negative in UHA and AHA throughout the hypokinetic period. Body weight and a food intake decreased significantly in SHA and UHA when compared with SCA and UCA. Significant losses of Mg in SHA and UHA occurred in the presence of Mg deficiency and suggest that prolonged HK induces another factor that influences Mg metabolism. We conclude that prolonged HK causes significant changes in Mg values of plasma, urine, and feces and a negative Mg balance in rats, despite Mg supplements leading to Mg deficiency.

Animals↗
PubMed1988

Availability of body magnesium during magnesium deficiency.

Extensive experimental and clinical studies in animals and humans during the past 25 years have yielded considerable data regarding the availability of internal magnesium (Mg) stores for the maintenance of extracellular and critical tissue concentrations of Mg during periods of Mg deprivation. The bulk of body Mg is present in bone and skeletal muscle, and it is these two sites that provide essentially all the available Mg. In the rat, approximately 15% of bone Mg (equivalent to 1.5 mmol/kg body weight) can be lost, whereas less than one tenth of that amount is available from skeletal muscle. In the human, up to 35% of bone Mg can be lost, but the mean loss in extant studies is 18% (equivalent to 1.2 mmol/kg body weight). In contrast to the rat, up to 40% of human skeletal-muscle Mg can be lost with an average loss of 15% (equivalent to 0.45 mmol/kg). In the human, the bone and skeletal-muscle Mg pools can provide an average of 1.7 mmol/kg body weight equivalent to 15% of total body Mg. Release of Mg from these stores appears to depend on the presence of hypomagnesemia which may also result in small, significant and potentially adverse Mg losses from certain vital organs such as the heart, kidney and brain. The liver and other organs appear not to lose Mg despite Mg deprivation although intracellular Mg shifts of importance cannot be ruled out. These data indicate that the body reserve to combat Mg depletion is not designed to protect the extracellular Mg pool and certain critical organs from Mg deficiency. A continuous optimal intake of Mg is needed for good nutrition and health.

Animals↗
PubMed1976

Magnesium deficiency in children with urolithiasis.

In a group of 57 children with urolithiasis hypomagnesaemia was found in 15 cases (26.3%). All children but one with abnormally low serum magnesium levels had recurrent or bilateral nephrolithiasis or nephrocalcinosis. Prevalence of hyperoxaluria and hypercalciuria, marked severity of the clinical features, abnormality of Ca metabolism and its responsiveness to MgO treatment were demonstrable in Mg deficiency.

Adolescent↗
PubMed1987

Renal magnesium wasting in a patient with short bowel syndrome with magnesium deficiency: effect of 1 alpha-hydroxyvitamin D3 treatment.

We studied a patient with severe hypomagnesemia due to small bowel resection who had marked renal magnesium (Mg) loss in response to iv Mg infusion. She had an undetectable serum 1,25-dihydroxyvitamin D [1,25-(OH)2D] level before treatment. Although Mg infusion increased her serum Mg levels and enhanced renal PTH action, as evidenced by an elevation in nephrogenous cAMP, the serum 1,25-(OH)2D level remained low. After the administration of 1 alpha-hydroxyvitamin D3, her serum 1,25-(OH)2D level increased, and fractional excretion of Mg decreased. With the elevation in serum 1,25-(OH)2D, serum Mg levels could be maintained without Mg infusion, although they were still subnormal. These results are consistent with the assumption that patients with the short bowel syndrome and Mg deficiency have reduced renal tubular Mg reabsorption which causes renal Mg loss, and that impaired tubular Mg reabsorption is due at least in part to deficient renal action of 1,25-(OH)2D. Because depressed serum 1,25-(OH)2D levels cannot be corrected rapidly by Mg infusion, administration of 1 alpha-hydroxyvitamin D3 or 1,25-(OH)2D3 appears to be the treatment of choice for Mg deficiency in patients with short bowel syndrome.

Adult↗
PubMed1998

Magnesium deficiency exacerbates brain injury and stroke mortality induced by alcohol: a 31P-NMR in vivo study.

Mimicking in rats the reduced level of dietary magnesium (Mg) intake, seen in present-day Western World populations, short-term (4 weeks) restriction of Mg intake (30-35% normal) resulted in a 40% loss in brain intracellular free Mg2+ ions ([Mg2+]i) and significant rises in brain intracellular pH (pHi) and phosphocreatine ([PCr]) but no change in [ATP] or [Pi] as measured by 31P-NMR spectroscopy. Such Mg-deficient animals (serum Mg fell 65%), when given ED40 stroke doses of ethanol, demonstrated a 100% stroke mortality. These findings indicate that: 1) moderate, short-term Mg deficiency makes the brain vulnerable to hypoxic-lethal stroke insults induced by alcohol administration, and 2) brain [Mg2+]i appears to play an important role in finely regulating brain pHi and [PCr].

Animals↗
PubMed2004

Magnesium deficiency inhibits primary tumor growth but favors metastasis in mice.

The results of several experimental and epidemiological studies have shown an inverse correlation between Mg status and the risk of some cancers. However, relationship between magnesium and cancer is complex. The aim of our work was to examine the precise effect of Mg deficiency on transplantable mouse tumor growth and metastasis. The results obtained indicate a significant retardation of primary tumor growth (up to 70%) in mice receiving Mg-deficient diet. However, Mg repletion caused in these mice significant increase of primary tumor burden. Analysis of cell cycle distribution showed a reduced percentage of cells in the S phase and an increase of cells in the G(0)/G(1) phase of the cell cycle in LLC tumors caused by Mg deficiency. This is in agreement with the effect of low Mg level on cell growth observed in vitro. Interestingly, in mice inoculated with LLC cells and receiving low-magnesium diet, a higher metastatic potential was observed as compared to control mice. In conclusion, our results demonstrate a direct role of magnesium in tumor growth and also point at deleterious effect of low magnesium status on tumor metastasis.

Adenocarcinoma↗
PubMed1990

Nephrocalcinosis without functional renal impairment in rats subjected to subacute moderate magnesium deficiency, and intervention studies on the mobilization of calcium deposits.

Female Sprague-Dawley rats (100-120 g) were kept for 12 d on diets containing 250, 1500, or 9000 ppm Mg. Then subgroups were loaded with water, frusemide or magnesium and urine was collected over 6 h. Moderately Mg-deficient diet (250 ppm) induced moderate hypomagnesaemia (62.3% of controls), but did not result in hypercalcaemia or the formation of typical erythema. Nevertheless, pronounced nephrocalcinosis developed, as shown by increased renal wet and dry weight and elevated tissue concentrations of Ca, P and Mg, the calculous deposits probably consisting to a large extent of Ca3 (PO4)2. Despite these alterations, renal function remained unimpaired in Mg-deficient rats, as shown by normal urinary creatinine excretion and the unaffected ability of the kidneys to concentrate urine. Loading with water, frusemide or Mg increased urinary excretion of calcium in all three diet groups to a similar extent; hence no significant proof can be given that calculous deposits are mobilized under these conditions. Since comparable conditions may also be present under clinical conditions in man, special care should be given to maintain optimal Mg balance.

Animals↗
PubMed1988

Effect of moderate magnesium deficiency on serum lipids, blood pressure and cardiovascular reactivity in normotensive rats.

1. Weanling Wistar rats were pair fed for 10 weeks on a purified diet containing either normal or suboptimal quantities of magnesium (960 or 80 mg/kg respectively). 2. At week 2, hypomagnesaemia was accompanied by hypertriglyceridaemia, an increase in plasma cholesterol and a decrease in high-density-lipoprotein-cholesterol in animals fed on the Mg-deficient diet. At week 10, the increase in triglycerides observed in Mg-deficient animals was less marked while the increase in total cholesterol was more important. 3. During the whole experimental period, Mg-deficient animals never showed hypertension. At week 2, mean arterial blood pressure was significantly lower in Mg-deficient rats than in their respective controls, while heart rate was significantly increased. However, hypotension accompanied by tachycardia was a transitory phenomenon which appeared only in the early phase of deficiency. 4. Vascular reactivity was studied in vagotomized anaesthetized rats after ganglionic blockade with pentolinium and atropine sulphate. The reactivity to noradrenaline was significantly higher in Mg-deficient rats compared with pair-fed controls after 2 weeks on the experimental diet.

Animals↗
PubMed1993

Vascular tissue anatomy of Norway spruce needles and twigs in relation to magnesium deficiency.

Vascular tissues of needles and twigs of Norway spruce with low foliar magnesium concentrations were examined by light microscopy. Observations were made on samples from (1) apparently healthy trees, (2) trees exhibiting progressive symptoms of decline, including the yellowing and fall of needles and the death of twigs and branches in the subapical canopy, and (3) trees recovering from symptoms of decline after fertilization with magnesium sulfate. Abnormalities in cambium and phloem anatomy, which were apparent in 2-year-old needles of declining trees, were seen only in needles at least 4 years old in healthy trees, suggesting that needles of declining trees are susceptible to precocious aging. Abnormalities in xylem anatomy were observed in needles 3 years or more in age in declining trees, but were never seen in needles of healthy trees. Over time, anatomical abnormalities in declining trees were seen in progressively younger twigs, which may explain the acropetal development of decline symptoms. After fertilization with magnesium sulfate, normal phloem and xylem were observed in the newly formed tissues.

Journal Article↗
PubMed1980

Blood and mast cell histamine levels in magnesium-deficient rats.

The number and morphology of mast cells (MCs) in the duodenal submucosa and the histamine content of blood and isolated peritoneal mast cells were estimated sequentially in male weanling Sprague-Dawley rats magnesium (Mg)-depleted for up to 48 days. Blood histamine levels increased 4--5-fold by 14 days of Mg depletion and subsequently declined to levels similar to those in pair-fed Mg-adequate controls. In the same period, the submucosal MCs continuously increased in number, beginning to plateau at 6--7 times the control number between days 36--48 of Mg deficiency. Massive MC degranulation was seen in the early stages of Mg-depletion but subsided after 16--20 days. Subsequently, the submucosal MCs appeared small and rounded. They showed reduced staining with toluidine blue indicating a deficiency in the mucopolysaccharide component of the storage granules. Histamine content of purified peritoneal MCs from Mg-deficient rats was reduced by 10 days of Mg depletion and remained at or below one-third the control level throughout the depletion period. The data suggest that the MCs remaining or developed during chronic Mg depletion are deficient in their capacity to store and secrete histamine.

Animals↗
PubMed2004

Magnesium deficiency and osteoporosis: animal and human observations.

Although osteoporosis is a major health concern for our growing population of the elderly, there continues to be a need for well-designed clinical and animal studies on the link between dietary magnesium (Mg) intake and osteoporosis. Relatively few animal studies have assessed the skeletal and hormonal impact of long-term low Mg intake; however, these studies have demonstrated that Mg deficiency results in bone loss. Potential mechanisms include a substance P-induced release of inflammatory cytokines as well as impaired production of parathyroid hormone and 1,25-dihydroxyvitamin D. Abnormal mineralization of bones may also contribute to skeletal fragility. Clinical studies have often varied greatly in study design, subject age, menopausal status and outcome variables that were assessed. Most studies focused on female subjects, thus pointing to the great need for studies on aging males. According to the U.S. Department of Agriculture, the mean Mg intake for males and females is 323 and 228 mg/day, respectively. These intake levels suggest that a substantial number of people may be at risk for Mg deficiency, especially if concomitant disorders and/or medications place the individual at further risk for Mg depletion. In this paper, we will review animal and human evidence of the association of Mg deficiency with osteoporosis and explore possible mechanisms by which this may occur.

Animals↗